Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Activation of Wnt signaling pathways in murine B16-F1 melanoma cells

ABSTRACT: Genome-wide transcriptional profiling using microarrays was used to compare gene regulation in B16 murine melanoma cells that were: 1) stably transduced with Wnt1-iresGFP; 2) stably transduced with Wnt3A-iresGFP; 3) stably transduced with Wnt5A-iresGFP; and 4) stably transduced with GFP and treated for 72 hours with 10 mM lithium chloride, a pharmacologic activator of canonical Wnt/beta-catenin signaling. Cells were sorted by fluorescence-activated cell sorting (FACS) to obtain populations with relatively equivalent levels of GFP expression. Biologic triplicates were used for each condition, and compared in two-channel hybridization to control RNA obtained from B16 cells expressing GFP (pooled from three biologic replicates).

ORGANISM(S): Mus musculus

SUBMITTER: Andy Chien

PROVIDER: E-MTAB-3012 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Activated Wnt/beta-catenin signaling in melanoma is associated with decreased proliferation in patient tumors and a murine melanoma model.

Chien Andy J AJ Moore Erin C EC Lonsdorf Anke S AS Kulikauskas Rima M RM Rothberg Bonnie Gould BG Berger Aaron J AJ Major Michael B MB Hwang Sam T ST Rimm David L DL Moon Randall T RT

Proceedings of the National Academy of Sciences of the United States of America 20090114 4

This study demonstrates that in malignant melanoma, elevated levels of nuclear beta-catenin in both primary tumors and metastases correlate with reduced expression of a marker of proliferation and with improved survival, in contrast to colorectal cancer. The reduction in proliferation observed in vivo is recapitulated in B16 murine melanoma cells and in human melanoma cell lines cultured in vitro with either WNT3A or small-molecule activators of beta-catenin signaling. Consistent with these resu ...[more]

PMID: 19144919

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Project description:Purpose: RNA-sequencing analysis defined a novel role for PRMT7 in melanoma cancer immunotherapy. Methods: PRMT7-deficient cells and control B16.F10 cells treated with mIFN-γ (100ng/ml) for 24 hours. B16.F10 melanoma cells mRNA profiles were generated by deep sequencing, in triplicate using TruSeq Stranded mRNA Sample Prep Kit with TruSeq Unique Dual Indexes (Illumina, Hiseq4000, SR75 platform located at San Diego, CA; UCSD IGM Genomics Facility, La Jolla, CA). Resulting libraries were multiplexed and sequenced with 100 base pair (bp) to a depth of approximately 30 million reads per sample. The sequence reads that passed quality filters were trimmed with Trimmomatic v0.39. STAR v2.7.1a was then used to align the reads to the mouse genome (mm10/GRCm38). Gene expression was quantified across all samples with HOMER v4.11.1, and the normalization was carried out through the regularized logarithm (rlog) transformation of DESeq2 v1.26.0. Differential expression between PRMT7 WT and knockdown samples were calculated through DESeq2 v1.26.0, and the gene expression was considered significantly different if the absolute value of the log-fold-change (LFC) was higher than 2, the base means larger than 10 and the false discovery rate (FDR) less than 0.05. Results: Differential expression analysis between the siLuc and siPRMT7 conditions yielded 185 and 251 genes with statistically significant differences and absolute fold change greater than 2 in the IFN– and IFN+ treatments respectively. Of these, 85% of genes are upregulated in the IFN– treatment, while 72% of genes are downregulated in the IFN+ treatment. Gene ontology analysis using the 185 and 251 lists of differentially expressed genes implies that the downregulated biological processes are enriched for the immune response pathways, while upregulated genes are more involved in the cell cycle process. Altered expression of some genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to better understand PRMT7 function in cancer immunotherapy. Conclusions: Our study represents the first detailed analysis of B16.F10 melanoma transcriptomes without PRMT7 expression, with biologic replicates, generated by RNA-seq technology. We conclude that RNA-seq based transcriptome characterization would expedite genetic network analyses and permit the dissection of PRMT7 biologic functions in modulating melanoma transcriptome.

Dataset Information

Activation of Wnt signaling pathways in murine B16-F1 melanoma cells

Publications

Activated Wnt/beta-catenin signaling in melanoma is associated with decreased proliferation in patient tumors and a murine melanoma model.

Similar Datasets

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